Scientists find hidden pulse in the brain that may predict Alzheimer’s disease
Scientists at the Mark and Mary Stevens Institute for Neuroimaging and Informatics (Stevens INI) at the Keck School of Medicine of the University of Southern California have created a groundbreaking brain imaging method that captures how the brain’s smallest blood vessels beat in time with each heartbeat. These subtle movements may provide vital insights into aging and conditions such as Alzheimer’s disease.
Published in Nature cardiovascular researchThe study provides the first non-invasive approach to measuring “microvascular volumetric pulsation” – the rhythmic swelling and contraction of small blood vessels – in living humans. Using high-field 7T magnetic resonance imaging (MRI), researchers found that these microvascular pulsations become stronger with age, especially in the deep white matter of the brain. This area is essential for communication between brain networks but is also vulnerable to decreased blood flow from distal arteries, which carry blood from the heart to external parts of the body. As these impulses intensify, they may interfere with brain function and contribute to memory decline and the development of Alzheimer’s disease.
“The arterial pulsation is like the brain’s natural pump, helping to move fluids and remove waste,” said Danny J.J. Wang, Ph.D., professor of neuroscience and radiology at the Keck School of Medicine and senior author of the study. “Our new method allows us to see, for the first time in humans, how the sizes of these small blood vessels change with aging and vascular risk factors. This opens new avenues for studying brain health, dementia, and small vessel diseases.”
Scientists have long known that stiffness and excessive pulsation in large arteries are linked to stroke, dementia, and small-vessel disease. However, until now, it has been almost impossible to observe these rhythmic changes in the brain’s smallest vessels without using surgical procedures limited to animal studies.
To overcome this, the USC team combined two advanced MRI techniques – vascular space occupancy (VASO) and arterial circulation labeling (ASL) – to monitor subtle shifts in microvascular volume throughout the cardiac cycle. The results revealed that older people show stronger microvascular pulsations in the deep white matter compared to younger individuals, and that high blood pressure exacerbates these effects. “These findings provide a missing link between what we see on macrovascular imaging and the microvascular damage we see in aging and Alzheimer’s disease,” said lead author Fanhua Guo, Ph.D., a postdoctoral researcher in Wang’s lab.
Excessive vascular pulsation may also disrupt the brain’s “glymphatic system,” a recently discovered network that removes waste such as beta-amyloid, a protein that accumulates in Alzheimer’s disease. Over time, interfering with fluid circulation may accelerate cognitive decline.
“The ability to measure these small vascular impulses in vivo is a crucial step forward,” said Arthur Tuja, director of the Stevens Institute at INI. “This technology not only advances our understanding of brain aging, but also holds promise for early diagnosis and monitoring of neurodegenerative disorders.”
The researchers are exploring how this method can be adapted for wider clinical use, including more common 3T MRI scanners. Future studies will test whether microvascular volumetric pulsation predicts cognitive outcomes and whether it could serve as a biomarker for early intervention in Alzheimer’s disease and related conditions.
“This is just the beginning,” Wang said. “Our goal is to move this from research laboratories to clinical practice, where it can guide diagnostic, prevention and treatment strategies for millions at risk of developing dementia.”
About the study
In addition to Wang, other authors of the study are Fanhua Guo, Chenyang Zhao, Chenyang Xu, Cai Gan, and Xingfeng Shao of Stevens INI, and Ning Jin of Siemens Healthcare.
This research was supported by National Institutes of Health (NIH) grants UF1-NS100614, S10-OD025312, R01-600 NS114382, R01-EB032169, RF1AG084072, R01-EB028297, R01-NS134712, and R01-NS121040.














Post Comment